The primary objective of the proposed project is to investigate the relationships between the amygdala and the hypothalamus with regard to the neural regulation of food intake. While hyperphagia can result from destruction of the ventromedial hypothalamus, neither a theory which attributes the overeating to a loss of inhibitory input to the ventrolateral hypothalamus nor the theory which attributes it to an irritative stimulation of that region is adequate to explain the development of hyperphagia. As a working hypothesis it is proposed that the organizaton of the neural regulation of food intake is primarily dependent upon the activity of the amygdala. Neuroanatomical and electrophysiological studies have shown that the amygdala sends a massive output to the hypothalmus and exerts a strong control over hypothalamic output. Lesions of the hypothalamus which affect food intake are also going to affect this amygdaloid output. Behavioral studies have indicated that the amygdala may be involved in the regulation of food intake. It therefore is possible that the lesion effects attributed to the disruption of hypothalamic mechanisms may also be due to the disruption of amyygdaloid mechanisms. To evaluate this possibility, hyperphagia- and non-hyperphagia-producing lesions will be made in the hypothalamus of rats and patterns of degeneration studied in the amygdala and its efferent pathways by using silver staining techniques and correlated with food intake. Similarly, amygdaloid multiunit activity will be recorded following various hypothalamic lesions and correlated with the amount of food intake. The neuroanatomical and electrophysiological studies will provide a data base for a final series of experiments in which the effects of restricted lesions and stimulation of the amygdala on eating behavior will be studied. Because hypothalamic lesions can have partially different effects on food intake in male and female rats, the different experiments will be done using both males and females to determine possible sex differences in neural organization that might support these behavioral differences.